Kasamatsu and Pettigrew (1979) have shown that intraventricular 6-OHDA given during monocular deprivation prevents the deprived eye from losing its ability to drive cells in the visual cortex. In the work published to date 6-OHDA has been shown to prevent the effects of monocular deprivation after 1 week of monocular deprivation preceded by light rearing. Protection from deprivation that begins without prior binocular experience or that lasts several months has been examined. Other work on monocular deprivation suggests, however, that the mechanisms underlying deprivation effects may depend on the duration of deprivation and on the presence of prior binocular experience. Therefore, we plan to replicate the results of Kasamatsu and Pettigrew and then go on to examine the limits of the protection afforded by 6-OHDA, using deprivation lasting several months and not proceded by binocular experience. Kasamatsu and Pettigrew state that the cells driven by the deorived eye after 6-OHDA treatment have normal receptive field properties. This result predicts that, if that cells in other visual areas are also normal. 6-OHDA treatment should protect the vision of the deprived eye. We plan to test this prediction by comparing the deprived eye visual acuity of kittens receiving 6-OHDA during deprivation with the deprived eye acuity of kittens receiving vehicle solution. This experiment will be repeated for short term deprivation, for long term deprivation, and for short term deprivation in the absence of prior binocular experience.